Acute Inflammation (Part 1): Vascular Permeability & Vasodilation

Inflammation is the process of inflammatory cells, plasma proteins, and fluid from the circulatory system traveling into tissue in response to cell injury or infection. Inflammation has a set of distinct phases. Generally speaking there is acute inflammation (which is analogous to the innate immune system) and chronic inflammation (which is analogous to the adaptive immune system).

Innate Immunity ~ Acute Inflammation

Adaptive Immunity ~ Chronic Inflammation

Acute Inflamation Chronic Inflammation

Acute inflammation can be broken down further into 3 different stages. The first part of acute inflammation is the Fluid Phase in which arteriole dilation and an increase in venule permeability allows fluid from the circulatory system to travel into the effected tissue. This phase also includes the activation of complement, creation of leukotrienes/prostaglandins, formation of bradykinin, and the activation of mast cells. The fluid phase begins immediately after tissue injury or infection. The next phase, which peaks at about 1 day after injury, is the Neutrophil Phase. The fluid phase causes hemodynamic changes that get neutrophils to travel into the effected tissue where they phagocytosis necrotic tissue and pathogens. The third stage of acute inflammation is the Macrophage Stage which peaks about 2 days after injury. Here macrophages do many of the same activities neutrophils are already doing. Finally, there is what I call Macrophage Management. Through the release of cytokines and direct interactions with other cells, macrophages “decide” what the next step is. If the problem has already been resolved by acute inflammation then healing or scar formation will be initiation. If acute inflammation was unsuccessful in removing the noxious stimuli, then macrophages can initiate chronic inflammation by acting as the antigen presenting cell for T cells. In some unique circumstances, additional acute inflammation is needed. Having prolonged periods of acute inflammation may seem counterintuitive, but acute and chronic inflammation are differentiated by their mechanism (not by the timeline).

 

Normally, there is no net flow of fluid between the vessels and the tissue. The amount of fluid flowing into the tissues equals the fluid flowing back into the vessel. However, during the fluid phase of acute inflammation there is a net flow of fluid into the tissue. The fluid phase is the beginning of acute inflammation and is the process of delivering blood and its contents to the site of injury/infection. It is brought about by two mechanisms; vessel injury and cytokine directed vasculature changes. Obviously if there is an injury that results in vessel damage, more blood is going to spill into the tissue because the integrity of the vascular wall is decreased. However, even if the vessels are intact more fluid is going to flow to the area because cytokines cause changes in vessels at the site of injury.

Venule Permeability Vasodilation Arteriole Dilation Acute Inflammation

Cellular injury and infection cause the release of histamine, prostaglandins, leukotrienes, and bradykinin. Additionally, the small number of Sentinel Macrophages that reside in tissue recognize the need for inflammation and send out cytokines of their own. Collectively, these cytokines trigger the fluid phase by dilating arterioles and increasing the permeability of the venules (pericytes contract opening small pores in the venule membrane). The dilation of the arteriole brings more blood to the area and the increased venule permeability means a greater proportion of the blood present ends up in the tissue.

3 thoughts on “Acute Inflammation (Part 1): Vascular Permeability & Vasodilation”

  1. This is Pathoma-level explanations. Good stuff and I really appreciate it. If you could toss in a key clinical example or classical presentation a bit more often, that’d be great!

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